Nitric oxide is the mediator of ATP‐induced dilatation of the rabbit hepatic arterial vascular bed

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Abstract
Livers of 10 New Zealand White rabbits were perfused in vitro with Krebs‐Bülbring buffer via the hepatic artery (HA) and portal vein (PV) at constant flows of 23 ± 1 and 77 + 1 ml min−1 100 g−1 respectively. The tone of the preparation was raised with noradrenaline (concentration: 10 μm). Dose‐response curves for the vasodilatation produced by adenosine 5′‐triphosphate (ATP), acetylcholine (ACh), adenosine, and sodium nitroprusside (SNP) were obtained following injection into the HA supply. Injections were then repeated in the presence of the l‐arginine to nitric oxide pathway inhibitors N‐monomethyl‐l‐arginine (l‐NMMA, n = 6) and N‐nitro‐l‐arginine methyl ester (l‐NAME, n = 4) at concentrations of 30 μm and 100 μm for each inhibitor. Both l‐NMMA and l‐NAME antagonized the responses to ATP and ACh; l‐NAME was 2–3 times more potent than l‐NMMA as an inhibitor of these endothelium‐dependent vasodilatations. Neither l‐NMMA nor l‐NAME attenuated responses of the endothelium‐independent vasodilators, adenosine and SNP. These results indicate that nitric oxide is the mediator of ATP‐induced vasodilatation in the HA vascular bed of the rabbit and that the receptor responsible for the release of nitric oxide, the P2y‐purinoceptor, is located predominantly on the endothelium.